Advances in targeting estrogen synthesis and receptors in patients with endometriosis.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and therapeutic targets without original data or systematic search
PubMed 36529967 · doi:10.1080/13543784.2022.2152325
What was done
This review summarized the molecular mechanisms underlying estrogen dependence in endometriosis lesions. The authors evaluated available and emerging interventions targeting estrogen pathways centrally (GnRH agonists and antagonists) and locally (aromatase inhibitors, steroid sulfatase inhibitors, and 17β-HSD1 inhibitors), as well as agents directly targeting estrogen receptors (SERMs, ER agonists, and ER antagonists).
What was found
No numerical data or quantitative outcomes are reported in the abstract. Existing treatments acting on systemic estrogen pathways induce hypoestrogenic side effects, exert contraceptive actions, and do not provide definitive cures. Preclinical and animal investigations of emerging ER-targeting compounds and local synthesis inhibitors show potential for lesion-specific suppression with reduced systemic side effects.
Why it matters
Standard hormonal therapies for endometriosis cause severe systemic hypoestrogenism and prevent pregnancy. Highlighting local enzyme inhibitors and receptor modulators outlines therapeutic pathways that may preserve systemic hormonal balance while inhibiting endometriotic implants.
Limits
As a narrative review, it lacks systematic search methodology, risk-of-bias assessments, and quantitative meta-analyses. The emerging treatments discussed rely predominantly on preclinical and animal studies, with human efficacy and long-term safety remaining to be established.
Cited by
- supports Ectopic endometriosis implants produce their own local estrogen.